CC BY
13
UDC 616.127-005.8-008.315:547.918:611.018.74:612.13 https://doi.org/10.26641/2307-0404.2018.2(part1).129519
O. Kuryata, A. Zabida, O. Sirenko
LEVELS OF GALECTIN-3, ADVANCED GLYCATED END-PRODUCTS IN SERUM, ENDOTHELIAL FUNCTION AND CARDIAC HEMODYNAMICS IN POST INFARCTION HEART FAILURE IN PATIENTS WITH REDUCED AND PRESERVED EJECTION FRACTION
SE «Dnipropetrovsk medical academy of Health Ministry of Ukraine»
Department of Internal Medicine 2
V. Vernadsky str., 9, Dnipro, 49005, Ukraine
ДЗ «Днтропетровська медична академiя МОЗ Укра'ти»
кафедра внутрiшньоi медицини 2
(зав. - д. мед. н., проф. О. В. Курята)
вул. В. Вернадського, 9, Днтро, 49005, Украта
e.mail: [email protected]
Key words: postinfarction chronic heart failure, galectin-3, AGEs, endothelial dysfunction, cardiac hemodynamics Ключовi слова: посттфарктна хронiчна серцева недостаттсть, галектин-3, AGEs, ендотелiальна дисфункцiя, серцева гемодинамiка
Abstract. Galectin-3, advanced glycated end-products serum levels, endothelial function and cardiac hemodynamics in post infarction heart failure patients with reduced and preserved ejection fraction. Kuryata O., Zabida A., Sirenko O. Epidemiological studies have reported that the rate of signs and symptoms of heart failure after myocardial infarction is approximately 25%. In addition, approximately 40% of myocardial infarctions are accompanied by left ventricular systolic dysfunction. Aim.. Aim of the study is to evaluate serum levels of galactin-3, AGEs and endothelial function, cardiac hemodynamics in post infarction chronic heart failure patients with different ejection fraction. Materials and methods. All patients are divided into two main groups according to ejection fraction:1st group-20 patients with chronic heart failure with preserved ejection fraction, 2nd group-15 patients with chronic heart failure and reduced ejection fraction. Standard laboratory blood tests for erythrocyte sedimentation rate, haematological parameters, lipid profile, glucose, renal function, echocardiographic examination, endothelial function determine were performed for all patients. AGEs and galectin-3 serum levels were determined. Results. Patients with chronic heart failure and reduced ejection fraction and myocardial infarction in anamnesis had significantly increased left ventricle diastolic volume, left ventricle systolic volume,left ventricle diastolic dimension and left ventricle systolic dimension (p<0.05).AGEs serum level mildly increased in both groups.Galectin-3 level was significantly higher in pts with chronic heart failure and reduced ejection fraction(p < 0.05)and was correlated with age(R=0.74, p<0.05), left ventricle end diastolic volume (R=0.57, p<0.05), left ventricle end diastolic dimension (R=0.48, p<0.05), triglycerides level (R=0.45, p < 0.05). Most of the patients with chronic heart failure with myocardial infarction in anamnesis had endothelial dysfunction, the FMD% level was significantly higher in patients with preserved ejection fraction(p<0.05). Conclusions. Patients with chronic heart failure and reduced ejection fraction are characterized by significantly higher levels of galectin-3, endothelial dysfunction frequency, cardiac hemodynamics abnormalities.
Реферат. PiBHi галектину-3, продукив кшцевот глжаци в сироватщ крош, функцюнальний стан ендотелм та серцева гемодинамша у хворих на серцеву недостатшсть шсля перенесеного шфаркту мюкарда 3i зниженою та збереженою фракщею викиду. Курята О., Забща А., Оренко О. Епiдемiологiчнi до^дження свiдчать, що симптоми серцево'1' недостатностi пiсля перенесеного тфаркту мiокарда мають Micце приблизно в 25% хворих. Крiм того, приблизно 40% iнфарктiв мюкарда супроводжуються систолiчною дисфункщею лiвого шлуночка. Мета до^дження - оцтити рiвень галектину-3, AGE в сироватщ кровi та ендотелiальну функцiю, серцеву гемодинамк в пацieнтiв is хронiчною серцевою недостаттстю пюля тфаркту зрiзною фракщею викиду. Матерiали та методи. 35 хворих з хрончною серцевою недостаттстю на тлi перенесеного тфаркту мюкарда вжом вiд 40 до 80 ротв були включен в до^дження. Пащенти були розnодiленi на двi оcновнi групи: 1-а група - 20 пацieнтiв -з хротчною серцевою недостатнютю зi збереженою фракщею викиду, 2-а група - 15 пацieнтiв i-з хротчною серцевою недоcтатнicтю зi зниженою фракщею викиду. Виконано стандартт лабораторт аналiзи кровi з визначенням гематологiчних параметрiв, лiпiдного профтю, глюкози, функцП нирок, ехокардiографiчне обстеження, визначення функщонального стану ендотелт. Визначено рiвнi AGEs та галектину-3 у cироватцi кровi. Результати. Пащенти iз хрончною серцевою недостатнютю та зниженою фракщею викиду на тлi перенесеного тфаркту мюкарда в анамнезi мали доcтовiрно вищi показники юнцевого дiаcтолiчного об'ему лiвого шлуночка, ктцевого cиcтолiчного об'ему
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OPHUHARbm ROCMRMEHHX
xieoгo wnywoHKa, кiнцеeого дiacmoxiннoгo posMipy xieoгo wnymHKa ma кiнцеeого cucmoxiннoгo posMipy xieoгo wnyHoHKa (p<0,05). PieeHb AGE y сироeamцi Kpoei 6ye n0MipH0 s6ixbweHuM e o6ox групaх. BcmaHoexeHo dcmoeipHO eu^uû pieeHb гaмeкmuнy-3 y xeopux 3 xpomHHom cep^eom HedocmamHicmm 3i SHuweHom ^pa^iem euKudy (p<0,05), w,o Kopexme 3 eiKOM (R=0,74, p<0,05), Ki^eeuM diacmoxiHHuM o6'eMoM мeoгo wnyHOHKc (R=0,57, p<0,05)), KiH^euM diccmoniHHUM posMipoM мeoгo wnymoHKc (R=0,48, p<0,05), pieHeM mp^xtyepudie (R=0,45, p<0,05). Eixbwicmb nc^eHmie 3 xpoHiHHom cep^eom HedocmamHicmm 3 iH^cpKmoM MioKcpdc e cHCMHesi Mam eHdomexicxbHy duc^yH^im, pieeHb eHdomeniûsanewHoï ea3oduMxm^ii 6ye docmoeipHo eu^UM y n^ieHmie si s6epeweHom ^pax^iem euKudy (p<0,05). Buchobku. Xeopi is xpoHiHHom cep^eom HedocmamHicmm ma SHuweHom ^pa^iem euKudy xapaKmepusymmbcx docmoeipHo eu^uM pieHeM гaмeкmuнy-3, nideu^eHom Hacmomom eHdomemanbHoï duc^yHK^ï, nopyweHb cep^eoï гeмoдuнaмiкu.
Epidemiological studies have reported that the rate of signs and symptoms of heart failure (HF) after myocardial infarction (MI) is approximately 25%. Importantly, this finding appears to be in agreement with the registries of several clinical trials. In addition, approximately 40% of myocardial infarctions are accompanied by left ventricular systolic dysfunction. Therefore, the available data suggest that HF after MI is a very frequent event [2]. Considering the type of cardiac dysfunction following MI, most patients present systolic dysfunction. Recent meta-analysis showed that restrictive mitral filling pattern, the most severe form of diastolic dysfunction, was presented in approximately 10% of the patients with preserved ejection fraction. In addition, restrictive pattern was associated with poor outcome [8]. However, the true prevalence and relevance of diastolic dysfunction after MI remains to be elucidated. Another important issue is that the consequences of cardiac dysfunction after MI are well established, and its presence increases the risk of death by at least 3- to 4-fold 6. Compared with patients without heart failure and left ventricular systolic dysfunction after myocardial infarction, patients who have heart failure and left ventricular systolic dysfunction are at higher risk for adverse outcomes, including cardiac rupture, cardiac arrest, stroke, longer hospitalizations, ventricular arrhythmias, recurrent myocardial infarction, and death, including sudden death [2].
Increasing HF severity is associated with NO imbalance and endothelial dysfunction that manifests in different forms [5]. Besides increasing afterload due to systemic [8] and pulmonary vascular constriction, altered endothelial function underlies regional vasomotor dysregulation in the renal and coronary circulation [14].
Decreased coronary of capacity vasodilator endo-thelium-dependent impairs myocardial perfusion, reduces coronary flow [7, 12], and worsens ventricular function [5]. The dysfunctional endothelium contributes to increased vascular stiffness and impaired arterial distensibility, augmenting myocardial damage [9, 10, 11]. NO imbalances also alter matrix metalloproteinases, which affect cell migration, cardiac hypertrophy, and atherosclerotic plaque stability [14].
Increased endothelin-1 in HF causes increased vascular resistance, smooth muscle cell growth, and matrix production, resulting in vascular remodeling, endothelial dysfunction, and HF progression. Reduced NO in HF affects endothelial progenitor cells, disabling endothelial repair and regeneration.
Advanced glycated end-products (AGEs) are end-products formed by oxidative and non-oxidative reactions between sugars and proteins [11]. AGEs form cross-links with long-living tissue proteins, which cause them to accumulate in the body over time. AGEs can bindto the receptor of AGE (RAGE) and thereby induce cardiovascular dysfunction [1] RAGE has a C-truncatedsecretory isoform, soluble RAGE (sRAGE), that circulates in plasma [17]. sRAGE has been proposed to have an atherosclerotic-protective function [4, 13]. However, AGE-RAGE interaction can also cause inflammation and increased AGE-accumulation.AGE-accumulation in turn can cause up regulation of RAGE [16]. Through decreased compliance of the heart and the vascu-lature, AGE accumulation is considered to be related to the onset and progression of HF [1].
Galectin-3 is a member of the family of soluble b-galactoside-binding lectins and it plays a crucial role in several diverse biological processes and diseases [12]. At the same time it is also associated with increased age, diabetic nephropathy, fibrotic conditions such as liver fibrosis [7], renal fibrosis, idiopathic lung fibrosis and chronic pancreatitis [15]. Recently it has drawn greater attention to its contribution in the pathophysiology of HF since it has been shown that galectin-3 promotes cardiac fibro-blast proliferation, collagen deposition, and ventricular dysfunction.
Aim of the study is to evaluate serum levels of galectin-3, AGEs and endothelial function, cardiac hemodynamics in post infarction chronic heart failure patients with different ejection fraction.
MATERIALS AND METHODS
Baseline Study
The study was conducted with the approval from the Ethics committee at State Establishment "Dnip-ropetrovsk medical academy of Health Ministry of
Ukraine" according to principles outlined in the Helsinki declaration.
Inclusion criteria: patients with myocardial infarction in anamnesis(>6 months) and chronic heart failure (HF) (ESC, 2016) aged from 40 to 80 years. Patients with acute myocardial infarction (<6 months), 2nd and 3rd degree heart block, diabetes mellitus (DM), renal failure (glomerular filtration rate: GFR<30 ml/min/1.73m2), hepatic failure, and cancer were excluded. All patients got standard treatment for HF according to ESC guidelines 2016 [6].
Standard laboratory blood tests for erythrocyte sedimentation rate, haematological parameters, lipid profile, glucose, renal and liver function tests were performed and body mass index (BMI) for all patients were calculated.
Echocardiographic examination was made by «VIVID 3», GE Medical Systems - USA in B, M, 2D, CFM, PW - mode pulse sensor 3S (3,5 MHz). Brachial artery measurement: brachial artery (BA) diameter, determining flow mediated dilatation (FMD)% and obtaining baseline and hyperemic BA flow velocities and deriving the respective flow volumes.
The fluorescent(f) AGEs in plasma were analysed by quantitative autofluorescence (fluorimeter Hoefer DQ 2000,USA) with fixed spectrum of excitation at 460 nm with 20% quinine solution as a standard with results expressed with conversion to glycated albumin.
Galectin-3 blood levels were measured by im-munoassay analysis using the "Human Galectin-3 Platinum ELISA" kit (GmbH, Austria) on the Stat Fax 2100 (USA) immunoassay plate analyser.
Statistical analysis
In order to accomplish the analysis of data, we used statistical program V.6.1 (StatSoft inc), and "Excel 2013" Microsoft. Data are shown as number of subjects (%) or median[interquartile range(IQR) because data are not normal distribution.
The Mann-Whitney U-test and Wilcoxon test were used to analyze differences between two independent and dependent groups respectively. Correlation coefficient Spearman (R) was calculated. A p value <0.05 was considered statistically significant.
Study design
First group (n=20) pts with HF and preserved ejection fraction (EF)>45% (HFpEF), second group (n=15) - pts with HF and reduced ejection fraction (EF)<45% (HFrEF).
RESULTS AND DISCUSSION
Clinical characteristics of patients were summarized in table 1.
Arterial Hypertension (AH) was estimated in 24 (69%) points, 1st degree - in 8 (23%), 2nd degree - in 16 (45%). Increased body mass index - in 22 (63%) pts, increased waist circumference -in 12 (34%).
Table 1
Baseline characteristics of the study population
1st group 2ndgroup
Characterstics Post infarction CHFpEF Post infarction CHFrEF
(n=20) (n=15)
p
value
Gender
Heartfailurefunctional class (NYHA), %
Age (years)
Body mass index (BMI) Heart rate (beat/minute) Atrial fibrillation (%) Arterial hypertension (%) Glomerular filtration rate (GFR) M±m
Blood glucose mmol/l M±m
Cholesterol mmol/l M±m
Triglycerides mmol/l M±m
Males(%) Females(%) 2nd FC 3rd FC M±m M±m M±m
17(85%) 3(15%) 12(60%) 8(40%) 59 [53;77] 28.4 [27.5;29.8] 72 [68;78] 5(25%) 17(85%) 84.4 [65.7;92.5] 5.2 [4.9;5.4] 4.9 [4.4;5.8] 1.7 [1.2;2.4]
13(87%) 2(13%) 4(27%) 11(73%) 66 [62;71] 27.7 [27;29.9] 76 [68;89.5] 6(40%) 8(51%) 86.6 [78.0;88.6] 5.5 [5.3;7.4] 4 [3.3;4.9] 0.9 [0.8;1.2]
0.023 0.145 0.312
0.153 0.098 0.031 0.027
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Postinfarction HFpEF patients had significantly higher cholesterol level and triglycerides (p<0.05). In the same time post infarction HFrEF patients were significantly older in age (p<0.05). There were no significant differences between the other indicators.
It was established significant differences between echocardiography indicators (table 2). Particularly, HFrEF patients with MI in anamnesis had significantly increasing levels of left ventricle end diastolic volume (LVEDV), left ventricle end systolic
volume (LVESV), left ventricle end diastolic dimension (LVEDD), left ventricle end systolic dimension (LVESD) on 37.6%, 62.3%, 18.5% and 33.3% respectively (p<0.05). The EF level was correlated with age (R=-0.72, p<0.05), the LVEDV level (R=-0.67, p<0.05), total cholesterol level (R=0.48, p<0.05), triglycerides level (R=0.42, p<0.05). There was significant correlation between LVEDD and age (R=0.68, p<0.05),GFR (R=-0.57, p<0.05).
Echocardiography parameters in both groups
Table 2
1st group 2ndgroup
Post infarction CHFpEF Post infarction CHFrEF P
(n=20) (n=15)
Left ventricle ejection fraction (EF) ,% M±m
57 [51.5;65]
40 [31;40.5]
0.003
Left ventricle end diastolic volume (LVEDV) ml M±m
133.5 [116.3;143.3]
214 [183;224.7]
0.006
Left ventricle end systolic volume (LVESV) ml M±m
53 [39.5;73]
140.5 [103;153.7]
0.021
Left ventricle end diastolic dimension (LVEDD) cm M±m
Left ventricle end systolic dimension (LVESD) cm M±m
Left atrium size (LAS) cm M±m
5.3 [5.0;5.4] 3.6 [3.4;4.1] 4 [3.9;4.2]
6.5 [6;6.7] 5.4 [4.7;5.6] 4.6 [4.3;5.0]
0.015
0.024
0.141
The median AGEs level was 1.6 [1.1;1.9]. There were no significant differences between AGEs level between study groups. The AGEs level correlated with GFR (R=-0.62, p<0.05), LVEDV (R=0.63, p<0.05). The median galectin-3 level was 6.9 [6.3;10.6], significant difference in galectin-3 level
was established depending on EF level in pts with HF (p<0.05) (table 3). The galectin-3 level was significantly higher by 12.5% (p<0.05) in pts with HFrEF and correlated with age (R=0.74, p<0.05), LVEDV (R=0.57, p<0.05), LVEDD (R=0.48, p<0.05), triglycerides level (R=0.45, p<0.05).
Table 3
Serum levels of AGEs and galectin-3 differences
* st 1st group 2nd group
Post infarction CHFpEF Post infarction CHFrEF
Advanced glycated end products (AGE)mg/ml 1.6 [1.4;1.9] 1.6 [1.2;1.8]
Galectin-3ng/ml 6.3 [5.8;9.1] 7.2 [6.9;10.8]
0.204
0.041
P
The FMD% level was significantly higher in 1st group pts. (fig.). The majority of patients with HFpEF, HFrEF and myocardial infarction in the anamnesis had endothelial dysfunction - 15 (75%)
and 15 (100%). The FMD% level correlated with age (R=-0.64, p<0.05), GFR (R=0.52, p<0.05), LVEDV (R=-0.63, p<0.05), galactin-3 level (R=-0.72, p<0.05).
FMD%
4,8
5 -
4
2,4
0
□ HFpEF □ HFrEF
FMD% level in pts with HF with different EF
CONCLUSION
1. HFrEF patients with MI in anamnesis had significantly increased left ventricle diastolic volume, left ventricle systolic volume, left ventricle dia-stolic dimension, left ventricle end systolic dimension.
2. AGEs serum level was mildly increased in patients with HFpEF and HFrEF.
3. Galectin-3 level was significantly higher in pts with HFrEF and correlated with age.
4. Most of the patients with HFpEF, HFrEF had endothelial dysfunction but the FMD % level was significantly higher in HFpEF pts.
REFERENCES
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3. Thijssen DHJ, Black MA, Pyke K, Padilla J, Atkinson GA, Harris RA, Parker B, Widlansky ME, Tscha-kovsky ME, Green DJ. Assessment of flow mediated dilation (fmd) in humans: a methodological and physiological guideline. Am J Physiol Heart Circ Physiol. 2011;300:H2-H12. doi: 10.1152/ajpheart.00471.2010
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6. Ponikowski P. et al. 2016 ESC Guidelines for the diagnosis and treatment The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure of the European Society of Cardiology (ESC) Developed in collaboration with the Heart Failure Association (HFA) of the ESC. European Heart Journal. 2016;37(27):2129-200. doi: 10.1093/eurheartj/ehs104
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ОРИГШАЛЬШ ДОСЛ1ДЖЕННЯ
14. Blair JE, Manuchehry A, Chana A, et al. Prognostic markers in heart failure - congestion, neurohormones, and the cardiorenal syndrome. Acute Card Care. 2007;9:207-13. https://doi.org/10.1080/17482940701606913
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round and round we go. Amino Acids. 2010;19. doi: 10.1007/s10741-010-9225-z
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СПИСОК Л1ТЕРАТУРИ
1. Advanced glycation endproducts (AGEs) and heart failure: pathophysiology and clinical implications / J.W. Hartog, A.A. Voors, S.J. Bakker, [et al.] // Eur. J. Heart. Fail. - 2007. - Vol. 9. - P. 1146-55. doi: 10.1016/j.ejheart.2007.09.009
2. Albert NM. Recognizing and managing asymptomatic left ventricular dysfunction: after myocardial infarction / N.M. Albert, C. Lewis // Crit. Care. Nurse. -
2008. - Vol. 28. - P. 20-37.
3. Assessment of flow mediated dilation (fmd) in humans: a methodological and physiological guideline / D.H.J. Thijssen, M.A. Black, K. Pyke, J. Padilla [et al.] // Am. J. Physiol Heart Circ Physiol. - 2011. - Vol. 300. -H2-H12. doi: 10.1152/ajpheart.00471.2010
4. Association between circulating soluble receptor for advanced glycation end products and atherosclerosis: observations from the Dallas Heart Study / J.B. Lindsey, J.A. de Lemos, F. Cipollone [et al.] // Diabetes Care. -
2009. - Vol. 32. - P. 1218-1220. doi: 10.2337/dc09-0053
5. Bauersachs J. Endothelial dysfunction in heart failure / J. Bauersachs, J.D.Widder // Pharmacol Rep. -2008. - Vol. 60. - P. 119-126.
6. ESC Guidelines for the diagnosis and treatment The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure of the European Society of Cardiology (ESC) Developed in collaboration with the Heart Failure Association (HFA) of the ESC / P. Ponikowski [et al.] // Eur. Heart. J. - 2016. - Vol. 37, N 27. - P. 2129-200. doi: 10.1093/eurheartj/ehs104
7. Galectin-3 modulates phagocytosis-induced stellate cell activation and liver fibrosis in vivo / J.X. Jiang, X. Chen, D.K. Hsu [et al.] // Am. J. Physiol Gastrointest Liver Physiol. - 2012. - Vol. 302. - P. 439-446. doi: 10.1152/ajpgi.00257.2011
8. Independentprognostic importance of a restrictive left ventricularfilling pattern after myocardial infarction: an individual patientmeta-analysis: Meta-Analysis Research Group in Echocardiographyacute myocardial infarction / J.E. M0ller, G.A. Whalley, F.L. Dini [et al.] // Circulation. - 2008. - Vol. 117. - P. 2591-2598. doi: 10.1016/j.amjmed.2005.08.010
9. Kuryata O.V. Effect of L-Arginine on the Serum Level of Advanced Glycation End Products in Patients with Post Infarction Chronic Heart Failure / O.V. Ku-
ryata, Abdunaser A. Zabida // J. Nutritional Therapeutics.
- 2017. - Vol. 6, N 2. - P. 43-50.
10. Kuryata O. Endothelial Function, Insulin Resistance, Serum Adiponectin Level in Rheumatoid Arthritis Females with RenalDysfunction and Its Dynamics with L-Arginine Aspartate Supplementation / O. Kuryata, O. Si-renko // Prensa Med Argent. - 2017. - Vol. 103. - P. 6.
11. Kuryata O. The inter relation of insulin resistance, serum adiponectin level in rheumatoid arthritis hypertensive females with subclinical atherosclerosis and its dynamics with the endothelial dysfunction correction // O. Kuryata, O. Sirenko / Orthop. Surgery Traumatol. -2017. - Vol. 1, N 5. - P. 162-173.
12. Liu F.T. Galectins: regulators of acute and chronic inflammation / F.T. Liu, G.A. Rabinovich // Acad Sci.
- 2010. - Vol. 1183. - P. 158-82. doi: 10.1111/j.1749-6632.2009.05131.x
13. Plasma levels of soluble receptor for advanced glycation end products and coronary artery disease in nondiabetic men / C. Falcone, E. Emanuele, A. D'Angelo [et al.] // Arterioscler Thromb Vasc Biol. - 2005. - Vol. 25. - P. 1032-7. doi: 10.1136/thx.2008.095588
14. Prognostic markers in heart failure - congestion, neurohormones, and the cardiorenal syndrome / J.E. Blair, A. Manuchehry, A. Chana [et al.] // Acute Card Care. -2007. - Vol. 9. - P. 207-213. https://doi.org/10.1080/-17482940701606913
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